Abstract Objective The study aimed to investigate the feasibility of establishing rhinosinusitis model in rats combinated with Lipopolysaccharide (LPS) and merocel sponge. Methods SD (Sprague Dawley) rats that underwent nasal obstruction using Merocel sponge packing, rats with LPS instillation alone, and rats with both nasal obstruction and LPS instillation were used to establish rat models of rhinosinusitis. After the models were established, the nasal symptoms of rats were recorded, the histopathological examination and Transmission Electron Microscopy (TME) of the sinus tissue were performed and the levels of Tumor Necrosis Factor-α (TNF-α), Interleukin-6 (IL-6) in the blood were also analyzed. The expressions of Aquaporin-5 (AQP5), Occludin, Toll-Like Receptor-4 (TLR4), Medullary differentiation factor 88 (MyD88) and phosphorylated (p)-p65 protein were detected by Western blot to evaluate the effect and mechanism of the experimental models. Results We found that compared with the control group and LPS group, the sinusitis symptom scores in the Merocel sponge combined with LPS group were significantly increased; the respiratory epithelia of the maxillary sinus were degenerated, cilia were detached, and even inflammatory cell infiltration occurred; the levels of TNF-α and IL-6 were increased; the expression of AQP5 and Occludin protein was decreased; and the expressions of TLR4, MyD88, and p-p65 protein were increased. Conclusion For the first time, we successfully established a rat rhinosinusitis model using Merocel sponge with LPS and explored the possible mechanism of LPS action.

Abstract Scutellarin, a flavonoid compound found in Scutellaria barbata, has been demonstrated to exert anti-cancer properity in a variety of human malignancies. However, its biological significance and underlying mechanism in glioblastoma (GBM) remain ambiguous. Network pharmacology approaches and molecular docking technologies were used to predict the crucial biological processes, candidate targets and signaling pathways of scutellarin against GBM. CCK-8, EdU, and colony formation experiments were performed to determine the effects of scutellarin on cell proliferation. Flow cytometry analysis was utilized to detect apoptosis. Western blot assays were used to measure the expression of proteins associated with EGFR-PI3K-AKT signaling. Through network pharmacology and molecular docking analysis, we found that EGFR might be a potential target and PI3K-AKT signaling might be the key signaling pathway for scutellarin to combat GBM. Scutellarin inhibited cell proliferation and induced apoptosis in a dose-dependent manner. Scutellarin also suppressed the phosphorylation level of EGFR in a dose-dependent manner. Scutellarin inactivated PI3K-AKT signaling by targeting EGFR. Moreover, scutellarin-mediated suppression of cell proliferation and increase of apoptosis was greatly reversed in GBM after overexpressing EGFR. Taken together, scutellarin is a novel inhibitor of EGFR-PI3K-AKT signaling to prevent GBM progression.